Insulin increases triglyceride secretion rate in rats in vivo.
Shinobu Satoh, Seiya Inoue, M Egawa, Yoshihiro Takamura, T Murase
Abstract
Shinobu Satoh, Seiya Inoue, M Egawa, Yoshihiro Takamura, T Murase
Abstract
To investigate whether insulin regulates triglyceride secretion from the liver in vivo, triglyceride secretion rate (TGSR) and serum insulin were measured in the following three experiments: in rats 12 weeks after ventromedial hypothalamic (VMH) lesions (Exp. 1), in rats 12 weeks after a high fat diet-feeding (Exp. 2), and in rats 10 days after streptozotocin treatment (65 mg/kg) (Exp. 3). Under hexobarbital anesthesia, overnight fasted rats were bled for measuring insulin and triglyceride. Rats were again bled 45 and 90 minutes after Triton WR 1339 (120 mg) injection, for measuring triglyceride. TGSR was calculated from serum triglyceride values measured before and after Triton injection. In Exp. 1, VMH obese rats had higher serum insulin concentrations and TGSR than control rats. There was a significantly positive correlation between serum insulin concentrations and TGSR in VMH lesioned rats alone (r = 0.939, P less than 0.001) and in VMH lesioned and control rats combined (r = 0.958, P less than 0.001). In Exp. 2, high fat diet-fed rats gained more weight than control rats, but they had the same levels of serum insulin concentrations and TGSR as those of control rats. In Exp. 3, streptozotocin treated rats had lower serum insulin concentrations and TGSR than control rats. There was a significantly positive correlation between serum insulin concentrations and TGSR in the two groups of rats combined (r = 0.680, P less than 0.05). From the results of these three sets of in vivo studies, we conclude that insulin increases TGSR in vivo.
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To investigate whether insulin regulates triglyceride secretion from the liver in vivo, triglyceride secretion rate (TGSR) and serum insulin were measured in the following three experiments: in rats 12 weeks after ventromedial hypothalamic (VMH) lesions (Exp. 1), in rats 12 weeks after a high fat diet-feeding (Exp. 2), and in rats 10 days after streptozotocin treatment (65 mg/kg) (Exp. 3). Under hexobarbital anesthesia, overnight fasted rats were bled for measuring insulin and triglyceride. Rats were again bled 45 and 90 minutes after Triton WR 1339 (120 mg) injection, for measuring triglyceride. TGSR was calculated from serum triglyceride values measured before and after Triton injection. In Exp. 1, VMH obese rats had higher serum insulin concentrations and TGSR than control rats. There was a significantly positive correlation between serum insulin concentrations and TGSR in VMH lesioned rats alone (r = 0.939, P less than 0.001) and in VMH lesioned and control rats combined (r = 0.958, P less than 0.001). In Exp. 2, high fat diet-fed rats gained more weight than control rats, but they had the same levels of serum insulin concentrations and TGSR as those of control rats. In Exp. 3, streptozotocin treated rats had lower serum insulin concentrations and TGSR than control rats. There was a significantly positive correlation between serum insulin concentrations and TGSR in the two groups of rats combined (r = 0.680, P less than 0.05). From the results of these three sets of in vivo studies, we conclude that insulin increases TGSR in vivo.
Key concepts: Endocrinology, Internal medicine, Triglyceride, Insulin, In vivo, Streptozotocin, Medicine, Diabetes mellitus